Diagnostic Tests for Coma
Coma Tests: Book Excerpts
Home Diagnostic Testing
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Coma Diagnosis: Book Excerpts
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Diagnostic Tests for Coma: Online Medical Books
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Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Coma.
DELIRIUM:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
Routine laboratory tests include a CBC, sedimentation rate, ANA, chemistry panel including electrolytes and BUN and VDRL tests, a blood alcohol level, urinalysis, and urine drug screen. A CT scan of the brain and EEG is usually indicated also. Acute delirium may be an indication to administer intravenous glucose and thiamine. If there is fever, blood cultures and a spinal tap for analysis and culture need to be done. Arterial blood gases and carboxyhemoglobin should be determined. Generally, a neurologist or neurosurgeon should be consulted early.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
SYNCOPE:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, VDRL test, thyroid profile, glucose tolerance test, EKG, and chest x-ray. Several blood pressure recordings in the recumbent and upright positions should be made. If hypoglycemia is suspected, a 72-hr fast and a tolbutamide tolerance test should be done. The drug history should always be reviewed. A toxicology screen may be helpful.
Most cases will require 24-hr Holter monitoring or event Holter monitoring. In addition, other cardiovascular studies, such as echocardiography and His' bundle studies, may need to be done. Exercise tolerance testing is useful when the syncope seems to be exercise induced. An upright-tilt test is helpful when vasodepressor syncope is suspected, especially when combined with isoproterenol infusion. Signal-averaged EKG can be useful if a ventricular arrhythmia is suspected. If transient ischemic attacks are suspected, a carotid scan and cerebral angiography may be necessary. If the syncopal attacks are thought to be due to epilepsy, a wake-and-sleep EEG may need to be done. A CT scan or MRI of the brain may need to be done.
A cardiologist or neurologist should be consulted before ordering expensive diagnostic tests. A psychiatrist may also need to be consulted.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
COMA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
When one encounters a patient with coma, the first thing to do is to establish an airway. Next, the blood pressure is taken. If there are any signs of shock, an intravenous access is established, and the shock is treated appropriately. A cardiology and surgical consult are obtained. Blood should then be drawn for a CBC, type and cross-match, sedimentation rate, chemistry panel, electrolytes, blood ammonia level, and blood alcohol levels. Before removing the syringe, 50 cc of 50% dextrose is given unless the patient is suspected of having hyperosmolar nonketotic diabetic coma. A urinalysis and urine drug screen must be done also. Arterial blood gas analysis should be done. If the situation is urgent or emergent, a CT scan is done before the results of the laboratory tests are available. If the laboratory tests are inconclusive, a CT scan must be done anyway.
If all of the above studies are negative, a spinal tap is done for cell count, protein, glucose, VDRL test, smear, and culture and sensitivity. This is especially true when there is fever or nuchal rigidity.
If the diagnosis is still in doubt, blood tests for other toxic materials, such as the lead level, and blood cultures and EEG are done. A neurologist or neurosurgeon is usually consulted as soon as one is available.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Level of consciousness, decreased:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because a decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Syncope:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?
Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Level of consciousness, decreased:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Syncope:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?
Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Delirium:
Physical examination.
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Because of the fluctuating nature of delirium, serial examinations are valuable.
A. Mental status. Observe the patient and take note of changes of level of consciousness, orientation, agitation, combativeness, hallucinations, or inability to concentrate. Evaluate the mental status by using the Mini Mental Status Examination (4) or a similar tool to standardize the findings (Chapter 4.5).
B. Physical status. Obtain vital signs and evaluate for clinical signs of dehydration, malnutrition, urinary retention, or fecal impaction. The physical examination should be guided by the history, keeping in mind the multifactorial nature of delirium. Evaluate for signs of infection, look for cardiopulmonary decompensation, and complete a thorough neurologic examination with special attention to identifying any focal neurologic deficit.
Testing
A. Laboratory. All patients should have a complete blood count, serum chemistries including electrolytes, hepatic and renal function, albumin and calcium, and a urinalysis. Additional studies will be directed by clinical suspicions based on the history and the physical examination. These may include thyroid studies, serum medication levels, serum and urine drug screens, lumbar puncture with spinal fluid studies, HIV status, syphilis test, vitamin B12 and folate levels, or serum markers of cardiac damage such as creatine kinase-MB or troponin.
B. Additional studies. All patients should have an electrocardiogram and a chest roentgenogram as well as arterial blood gases or oxygen saturation level tests. With no history of trauma or focal neurologic deficit, a computed tomography scan is of limited value. An electroencephalogram is also of limited value unless the diagnosis of seizure is being considered.
Diagnostic assessment.
Delirium can be a medical emergency, and a high index of suspicion must be maintained to accurately diagnose and treat the condition. Diagnosis is complicated by the similarity of presentation of depression, dementia and delirium, and by overlapping signs and symptoms. It is essential to rule out an underlying dementia or depression before the diagnosis of delirium can be made. This has particular impact on the treatment and prognosis of the illness.
A. Dementia is characterized by a gradual onset of decreased functioning in the areas of memory, execution of the activities of daily living, and social functioning. It is less likely for delirium to cause changes in sensorium, cognition, attention; it is also less likely for delirium to fluctuate from hour to hour. Delirium can coexist with an underlying dementia and should always be considered when a previously diagnosed dementia patient exhibits an acute change in mental status.
B. Depression is characterized by a depressed mood with psychomotor retardation or agitation. Look for a gradual onset of anhedonia, sleep disturbances, fatigue, feelings of guilt or worthlessness, or a previous history of depression (Chapter 3.3).
C. Other diagnoses. Consider in the differential diagnosis functional psychosis and bipolar disease, especially the manic phase. Both can produce hallucinations, although those of delirium tend to be visual or tactile, whereas those of psychosis tend to be auditory in nature. Epilepsy, especially temporal lobe seizures, can mimic delirium. Multi-infarct dementia, with its characteristic labile emotional state, must be considered. Remember that delirium is a complex, multifactorial condition and can present superimposed on a variety of other medical psychiatric conditions. A careful history and physical examination will help clarify the diagnosis and guide the physician and patient toward the correct treatments.
References
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: American Psychiatric Association, 1994:129–133.
2. Johnson JC. Delirium in the elderly. Emerg Med Clin North Am 1990;8:255–265.
3. American Psychiatric Association Practice Guidelines. Am J Psychiatry 1999;
156:S1–S20.
4. Folstein MF, Folstein SE, McHugh PR. Mini-mental status examination: a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189–198.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Syncope:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
What are the essential aspects to cover?
A. General: mental status, temperature, hydration status, pallor, or cyanosis.
B. Vital signs: tachycardia, bradycardia, irregularity, or orthostatic hypotension.
C. Cardiovascular: heart sounds, murmurs, bruits, edema, rales, and pulses.
D. Neurologic: cranial nerves, reflexes, strength and sensation, tremor, Romberg’s sign, gait, and cerebellar signs.
Testing.
Which tests are useful in diagnosing syncope?
A. Electrocardiogram (ECG). The most important single initial test to evaluate syncope is the ECG; it is easy and inexpensive and can quickly identify life-threatening arrhythmias or ischemia. Although the diagnostic yield is only 5% (3), if the ECG is normal, ischemia, arrhythmias, and organic heart disease are very unlikely (5). If the ECG is abnormal but does not clearly demonstrate a likely cause for syncope (complete heart block or runs of ventricular tachycardia, for example), other tests are needed to clarify the underlying problem that may be related to the syncope. The result of the ECG, therefore, helps to direct the course of further workup.
B. Cardiac monitors
1. Holter monitor or telemetry performed for 24 hours. For patient with organic heart disease, this gives a diagnostic yield of from 2% for arrhythmias correlated to symptoms to 21% with unrelated arrhythmias. Extending this monitoring to 72 hours is not useful (5).
2. A loop event monitor is a portable, prolonged ambulatory event recorder indicating if there is recurrent syncope and no organic heart disease (yield = 24% to 47%) (4).
C. Electrophysiologic studies. This invasive cardiac monitoring and arrhythmia induction procedure gives a 50% diagnostic yield for those with organic heart disease or abnormal ECG (compared with 10% if no organic heart disease) (4). This is considered the gold standard for arrhythmia diagnosis but it is expensive and invasive. Powerful predictors of a positive test are an ejection fraction less than 40%, bundle branch block, or atrial fibrillation (5).
D. Tilt table testing is indicated for unexplained, recurrent syncope when arrhythmia or organic heart disease is excluded and neurocardiogenic syncope is suspected. In this setting, the sensitivity is 67% to 83% and specificity is 90% (4).
E. Echocardiogram and stress tests are used only to evaluate exertional symptoms (echo first in this case) or suspected organic heart disease.
F. Computed tomography scan is used to evaluate focal neurologic signs.
G. Electroencephalogram is indicated for seizure activity only (Chapter 4.7).
H. Carotid massage. Consider this if the patient is aged more than 60 years with unexplained syncope. Perform in the clinic if no bruits, ventricular tachycardia, recent stroke, or myocardial infarction.
I. Blood tests, including hematocrit, serum chemistries, and pregnancy test, are not for screening; order only if a specific medical condition is suspected.
J. Psychiatric evaluation is useful in the setting of a high recurrence rate in a young patient without resultant injuries and no evidence of organic heart disease.
Diagnostic assessment.
The keys to the diagnosis of syncope are the history, physical examination, and ECG, yielding a diagnosis 45% of the time. The history and physical should focus on cardiac, neurologic, and medication-related issues. Directed testing can add 8% to diagnosis (3). Further classification by age and presence of organic heart disease can help focus evaluation and treatment. If organic heart disease is present or the ECG is abnormal, inpatient telemetry monitoring and electrophysiologic studies are recommended. If organic heart disease is not evident, ambulatory loop ECG and psychiatric evaluations are indicated, as well as possible tilt table testing (4).
Although most syncope patients can be evaluated in the outpatient setting, hospitalization is recommended for those with organic heart disease, chest pain, a history or suspicion of arrhythmia, or presence of neurologic symptoms or signs suggesting transient ischemic attack or stroke. The extent of severity of the organic heart disease is the key determinant of mortality and should direct evaluation and therapy (2). Despite extensive evaluation and testing, the diagnosis may still be elusive in approximately 40% of patients with recurrent syncope, but fortunately these patients have a low incidence of morbidity and mortality.
References
1. Grubb BP, Kosinski D. Neurocardiogenic syncope and related syndromes of orthostatic intolerance. Cardiology in Review 1997;5:182–190.
2. Kapoor WN, Hanusa BH. Is syncope a risk factor for poor outcomes? Comparison of patients with and without syncope. Am J Med 1996;100:646–655.
3. Linzer M, Yang EH, Estes NA 3rd, et al. Clinical guideline: diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med 1997;126:989–996.
4. Linzer M, Yang EH, Estes NA 3rd, et al. Clinical guideline: diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med 1997;127:76–86.
5. Meyer MD, Handler J. Evaluation of the patient with syncope: an evidence based approach. Emerg Med Clin North Am 1999;17:189–201.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Coma:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. A thorough general examination, including vital signs, helps to establish and rule out potential causes of coma. Look for evidence of head trauma or metabolic encephalopathy.
B. Neurologic examination. A detailed neurologic examination, including mental status; motor, sensory, reflex coordination; gait; and cranial nerve testing, will help distinguish the location and degree of dysfunction. Look for the following important features:
1. Level of consciousness. Is the patient responsive at all? To what degree?
2. Brainstem function
a. Pupils: assess cranial nerves (CN) 2 and 3 for anisocoria, miosis, pinpoint, mydriasis, or fixed, midposition pupils.
b. Eye movements: assess conjugate gaze, gaze deviation, nystagmus, and spontaneous movements (CN 3, 4, and 6).
c. Funduscopic examination: assess for papilledema and underlying diseases. Corneal reflexes (CN 5 and 7); gag and cough reflexes (CN 9 and 10).
3. Breathing patterns. Cheyne-Stokes respiration suggests cerebral hemispheric or diencephalic injury or an encephalopathy (hypoxic or metabolic). Central hyperventilation suggests brainstem injury. Ataxic or Biot’s respiration, which can progress to apnea, suggests injury to the reticular formation in the medulla and pons.
4. Sensorimotor activity. Are there spontaneous, volitional movements? Is there other motor activity such as choreoathetosis, decerebrate or decorticate activity, myoclonus, asterixis, or seizure activity? Is the muscle tone flaccid, rigid, spastic, or clonic? Is the response to painful stimuli purposeful, flexion withdraw, abnormal posturing, or no response at all?
5. Tendon reflexes. Are the reflexes asymmetric, increased, or decreased?
6. Glasgow Coma scale. Measures the depth and duration of altered consciousness based on the best response to three actions: eye opening, verbal response, and motor response to commands or painful stimulus.
Testing
A. Clinical laboratory tests. Complete chemistry profile (including electrolytes, glucose, calcium, magnesium, creatinine, blood urea nitrogen), complete blood count, coagulation panel, arterial blood gas, toxicology screen (blood, urine, gastric contents), thyroid function tests, cortisol level, and select cultures (blood, urine, throat, rectal, spinal fluid). Consider performing lumbar puncture after obtaining a computed tomography (CT) scan.
B. Diagnostic imaging. Cerebral CT findings reliably suggest intracranial hemorrhage, cerebral edema, mass lesions, focal infection, or hydrocephalus as diagnoses. Magnetic resonance imaging is preferred for the detection of abscess, tumor, subdural empyema, inflammatory lesions, or demyelinating diseases.
C. Other testing. Electroencephalography rules out seizures, status epilepticus (SE), and nonconvulsive SE. Lumbar puncture, typically after diagnostic imaging, may help determine increased intracranial pressure as well as infectious causes. Evoked potentials, such as brainstem auditory or short-latency somatosensory, provide information about the physiologic state and response to therapy (4).
Diagnostic assessment.
The prognosis in comatose patients is typically poor except for those that are drug-related or result from traumas. In general, the longer the coma lasts, the poorer the prognosis. Coma rarely lasts longer than 4 weeks, after which, transition into a vegetative state or recovery occurs (3).
References
1. Plum F, Posner JB. The diagnosis of stupor and coma, 3rd ed. Philadelphia: FA Davis, 1983.
2. Feske SK. Coma and confusional states: emergency diagnosis and management. Neurol Clin North Am 1998;16:237–256.
3. Giacino JT. Disorders of consciousness: differential diagnosis and neuropathic features. Semin Neurol 1997;17:105–111.
4. Chiappa KH, Hill RA. Evaluation and prognostication in coma. Electroenceph Clin Neurophysiol 1998;106:149–155.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Syncope:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The cause of syncope is usually evident after a careful history and physical exam. Identification of a cardiac cause is critical because it portends a poor prognosis (1-year mortality 18% to 33%). In patients with heart disease, the most specific predictors of a cardiac cause are syncope in the supine position or during effort, blurred vision, and convulsive syncope. In patients without heart disease, palpitations are the only significant predictor of a cardiac cause.
Focus on preceding events and witness description. Sudden loss of consciousness without warning is usually due to an arrhythmia. Syncope with chest pain mandates that aortic dissection, myocardial infarction, and pulmonary embolism be ruled out. Syncope with exertion suggests aortic stenosis, hypertrophic obstructive cardiomyopathy, or bradycardia. Events after the syncope, such as confusion, lethargy, or neurological symptoms suggest a seizure.
Consider syncope as the cause of unexplained trauma such as hip fracture or MVA.
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Source: Field Guide to Bedside Diagnosis, 2007
Coma:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Coma is a state of pathological unconsciousness, where the patient is unaware of their environment and unarousable. It is caused by dysfunction of either the reticular activating system above the level of the mid-pons or both cerebral hemispheres. It should be distinguished from brain death due to cessation of cerebral and cerebellar function, marked by absense of response to stimuli, respiratory drive, and central reflexes (although spinal reflexes may be preserved), and from persistent vegetative state, characterized by diurnal wakefulness but with unawareness and inability to interact with others.
Pupils: Pupillary responses are more sensitive than papilledema in detecting increased intracranial pressure. Normal pupils imply an intact midbrain and CNIII. Preserved pupillary light reflex with other signs of brainstem impairment suggests a toxic/metabolic cause. Asymmetric reactivity is consistent with an acute structural process. A unilaterally dilated pupil suggests ipsilateral uncal herniation. Hypothermia, barbiturates, and midbrain lesions produce midposition unreactive pupils. Pinpoint pupils occur with pontine lesions and opiates. Bilateral dilated unresponsive pupils occur with anoxia, severe midbrain damage caused by transtentorial herni-ation, or anticholinergic drugs. Large pupils that dilate and contract automatically (hippus) but do not react to light suggest a tectal lesion.
Eye deviation: Injection of ice water into the ear (calorics) normally causes deviation of both eyes toward the stimulated ear. Its absence implies dysfunction of the pons or medulla. Cortical mass lesions produce ipsilateral conjugate deviation that can be overcome with calorics. Brainstem and pontine lesions produce contralateral deviation that cannot be overcome with calorics. In metabolic coma or drug overdose coma, eyes move loosely side-to-side opposite the turning of the head. A pontine or cerebellar lesion causes skew deviation (separation of horizontal axes). Ocular bobbing (briskly down, slowly up) is a result of bilateral pontine lesions. Ocular dipping (slow arrhythmic downstroke, followed by a faster upstroke) with normal calorics is consistent with anoxic encephalopathy.
Posturing: Decorticate posturing (arm flexion and leg extension) is found with hemispheric lesions or metabolic derangement. Decerebrate posturing (extension of the legs and arms) implies dysfunction of the midbrain or upper pons on a structural or metabolic basis. In response to noxious stimuli, flexion, extension, and adduction reflexes are found. Shoulder and hip abduction involve cortical activity whereas withdrawal implies voluntary behavior.
Respiratory pattern: If the patient is yawning or swallowing, coma is not very deep and brainstem function is intact. Cheyne-Stokes respiration (crescendo-decrescendo pattern with apneic pauses) is seen with herniation, metabolic encephalopathy, and congestive heart failure. Central neurogenic hyperventilation (rapid deep breathing) indicates damage to the brainstem between the midbrain and pons. Ataxic respiration occurs with midbrain lesions. Apneustic respiration with inspiratory pauses occurs with pontine lesions and precedes respiratory arrest.
Asymmetric resting muscle tone, deep tendon reflexes, or Babinski response suggests a structural lesion. A toxic/metabolic cause is suggested by preceding confusion, disorientation, and somnolence. Myoclonic jerks or clonus provide further support.
The Glasgow Coma Scale is scored as follows: Best Motor Response: 6 obeys commands, 5 localizes pain, 4 withdraws to pain, 3 decorticate (flexion), 2 decerebrate (extension), 1 none. Best Verbal Response: 5 oriented, 4 confused conversational, 3 inappropriate words, 2 incomprehensible sounds, 1 none. Eye Opening: 4 spontaneous, 3 to speech, 2 to pain, 1 none.
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Source: Field Guide to Bedside Diagnosis, 2007
Delirium/Hallucinations:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Delirium is characterized by gross disorientation in the presence of alertness and vigilance, disorders of perception with vivid illusions, and psychomotor and autonomic hyperactivity. It usually develops over a short time and is associated
with fluctuating mental status, decreased attention, disorganized thinking as indicated by rambling, irrelevant, or incoherent speech, and a decreased level of consciousness. The most sensitive findings are variability in level of arousal, impaired short-term memory (e.g., digit span), and disorientation to time. Relatives or friends are helpful sources of information about the tempo and degree of impairment.
Fever, tachycardia, or hypertension should prompt a careful evaluation for a medical cause. Infection is a common cause in the elderly, especially pneumonia or urinary tract infection. Visual hallucinations are organic in origin, due to factors such as drugs, rather than due to schizophrenia.
Confusion Assessment1) Change in mental state (from baseline) that is acute and fluctuates. 2) Difficulty focusing attention or trouble keeping track of what is said. 3) Disorganized thinking (rambling or irrelevant conversation, unpredictable switching between subjects, illogical flow of ideas). 4) Altered level of consciousness (lethargy, stupor, or hyperalert). A positive test requires 1 and 2 positive, and either 3 or 4.
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Source: Field Guide to Bedside Diagnosis, 2007
Level of consciousness, decreased:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Decreased LOC can result from a disorder affecting virtually any body system. After performing a complete neurologic examination, let the results of your history guide the rest of your physical assessment.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Take the patient’s vital signs and examine him for any injuries that may have occurred during his fall. Then perform a complete cardiac and neurologic assessment.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope and Dizziness:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome. Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Alteration in Consciousness:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
When individualpresents with alteration of consciousness, diagnosis and treatment mustproceed concurrently, not serially.ABCs of resuscitation (airway, breathing,circulation) take precedence over other diagnostic and therapeuticmeasures. Airway must be cleared, and oxygen should be given bymask and bag ventilation.Failure of adequate ventilation requiresintubation.Hypotension or shock should be treatedwith volume expansion.With suspected or known head or necktrauma, head should be stabilized until lateral cervical spine radiographcan be performed to determine whether cervical spine injury hasoccurred.Level of consciousness and responsiveness,motor function, pupil size and responses, and extraocular movementsshould be evaluated. Presence or absence of meningeal signs as wellas focal hemispheric or brainstem findings also should be noted.Unless diagnosis has been establishedby history and physical exam, a number of tests need to be performed.Measurementof blood glucose should be done immediately at bedside.Blood should be sent for CBC with differential;serum electrolytes, glucose, creatinine, calcium, magnesium, ammonia;blood urea nitrogen; liver function tests; blood culture; and toxicology screen.Urine should be obtained for UA, urineculture, and toxicology screen. Vital Signs
Respiratory Rate and Pattern
Dyspneaand/or tachypnea may occur with pneumonia, any cause ofmetabolic acidosis, and lesions of lower midbrain–upperpontine tegmentum.Slow, irregular respirations may beassociated with drug intoxication, septicemia, and intracranialmass lesion. With acute head injury or diffuse brain damage of anycause, abnormal breathing patterns often overlap, making it difficultto relate specific pattern with discrete location of brain damage. Heart Rate
Bradycardia,if associated with hypertension and periodic breathing, suggestsincreased intracranial pressure.Tachycardia may occur with hypovolemicshock (dehydration, blood loss, diabetic ketoacidosis) and anticholinergicpoisoning. Blood Pressure
Hypertensionmay occur with increased intracranial pressure and with drug overdoses (amphetamines,cocaine, phencyclidine).Hypotension may occur with hypovolemia(fluid losses from gastroenteritis, acute blood loss, diabetic ketoacidosis),septicemia, adrenal insufficiency, and ingestion of alcohol or barbiturates. Temperature
Hyperpyrexiamay indicate presence of infection (bacterial meningitis, septicemia, pneumonia),heat stroke, or cocaine overdose. Although uncommon, brain lesionthat has disturbed temperature-regulating center also may producehyperpyrexia.Hypothermia may occur with severe hypovolemiaas well as with barbiturate or alcohol ingestion. Level of Consciousness and Responsiveness
Level ofconsciousness can be determined by noting degree of arousability.Response to name, simple commands,or painful stimuli (sternal pressure or pinching side of neck, innerarm, or thigh) can be used to evaluate degree of unresponsiveness.Eye opening or any form of speakingincluding grunting or groaning suggests some degree of functionof reticular activating system.Speech and purposeful withdrawal orlocalization of painful stimuli are signs of intact cortical function. Motor Function
Restlessmovements of arms and legs, variable resistance to passive movement,complex avoidance movements, and discrete protective movements generallyindicate intact corticospinal tracts, whereas asymmetry of functionmay indicate hemiparesis.Presence of posturing should be noted.Decorticate posturing consists of flexion of arms, wrists, and fingerswith adduction of upper extremities, and extension, internal rotation,and plantar flexion of lower extremities. Associated with diffusedamage to cerebral cortex and subcortical white matter or basalganglia. Decerebrate posturing, which consists of arm and hand extensionand back arching, is associated with extensive midbrain damage.Flaccid extremities and absence ofany motor response indicate further depression of brainstem function. Pupil Size and Responses
Exam ofpupils and their reactivity help determine level and location oflesions affecting reticular activating system in brainstem. Anyreactivity signifies intact parasympathetic and sympathetic pathwaysof oculomotor nerve. Bilateral lesions of midbrain that interruptthis pathway produce dilated unreactive pupils. Pontine lesionsproduce miotic pupils with only mild reaction to light. Unilateral pupillarydilatation suggests third nerve compression and impending uncalherniation.Generally, pupils remain reactive withmetabolic or toxic causes of coma. Exceptions include atropine orscopolamine poisoning, which causes dilated unreactive pupils; glutethimidepoisoning, which may cause medium to large unreactive pupils; opiatepoisoning (morphine, heroin), which causes pinpoint pupils withonly slight constriction to light; and severe anoxia with cardiacarrest, which produces fixed and dilated pupils. Miosis is usuallyseen with opiate, organophosphate, or clonidine overdosage, whereasmydriasis is usually seen with anticholinergic poisoning (tricyclicantidepressants) or with stimulant overdosage (amphetamines, cocaine). Extraocular Movements
Evaluationof eyes at rest, abnormal spontaneous eye movements, and ocularresponse to labyrinthine function provide important informationin assessment of alteration of consciousness.Cerebral lesions (usually frontal lobe)usually produce conjugate deviation of eyes to side of lesion andnormal labyrinthine responses, whereas unilateral pontine lesionsusually produce eye deviation away from side of lesion as well asabnormal labyrinthine responses. Midbrain lesions that involve oculomotornucleus or nerve or pontine lesions involving abducens nucleus ornerve may cause abduction of ipsilateral eye.Ocular response to vestibular stimulationalso helps evaluate integrity of brainstem function in childrenwith alteration of consciousness. Brainstem function is intact whenice water injection of 50 mL into external auditory canal with headflexed to 30 degrees produces conjugate horizontal eye deviationto side of injection and horizontal rapid nystagmus to oppositeside. Absence of such reflexes indicates severe brainstem dysfunction.Oculocephalic (doll's eye)reflex is also used to produce vestibular stimulation, but it iscontraindicated with suspected cervical spine injury. Head is rotatedfrom side to side and positive response indicating intact brainstemfunction is conjugate horizontal eye movement in opposite directionfrom head turn. Further Evaluation and Specific Diagnosis
Vital signsand assessments already described usually indicate whether any focal hemisphericor brainstem dysfunction exists. Final task is to make definitivediagnosis.Focal neurologic signs including asymmetricmovements and abnormal postures usually signify structural lesionin cerebral hemisphere, which also may affect brainstem function.Lesions above tentorium may cause alterationof consciousness by depression of large portions of both cerebralhemispheres, whereas lesions below tentorium (usually tumor or collectionof blood in posterior fossa) depress consciousness by compressionof brainstem structures.Presence of increased intracranialpressure may lead to central or uncal cerebral herniation. Centralherniation refers to rostrocaudal pattern of deterioration withloss of consciousness and irregular respirations followed by bilateraldilated unresponsive pupils and either decorticate or decerebrateposturing. Uncal herniation occurs more suddenly with loss of consciousnessand unilateral dilated pupil occurring almost simultaneously.Hemiparesis or hemiplegia may occurcontralateral to lesion.In cases of suspected structural lesion ± historyof head trauma, CT should be performed immediately. When herniationor impending herniation is suspected, patient should be intubated,hyperventilated, and given mannitol to acutely decrease increasedintracranial pressure prior to CT.Meningeal signs (stiff neck, Kernigor Brudzinski signs) commonly occur with bacterial meningitis andsubarachnoid hemorrhage. Lumbar puncture should be performed withsuspected bacterial meningitis or viral encephalitis. CT shouldbe performed first to rule out mass lesion in individuals with focalneurologic signs or symptoms of coma. If patient is unstable, appropriateantibiotic therapy should be given for suspected bacterial meningitisafter blood culture has been drawn, and lumbar puncture may be deferreduntil child is stable. In individuals with suspected subarachnoidhemorrhage and increased intracranial pressure, CT should be performedimmediately.Individuals without meningeal or focalneurologic signs may have head injury, drug intoxication, seizure,or metabolic disorder. Precise drug history is important but oftenis unavailable. 3 specific antidotes are available:Naloxone foropiate overdosePhysostigmine for anticholinergic poisoningFlumazenil for benzodiazepine overdose Metabolic causes of coma tend to producesymmetric hemispheric responses with normal brainstem function.With hyperammonemia in neonatal period,urea cycle defects and organic acid disorders should be suspected. Fig.3.1 (Adapted from Batshaw ML. Inborn errors of ureasynthesis. Ann Neurol 1994;35:137, with permission.) provides schemeto determine cause of hyperammonemia in neonates. Measurement ofserum ammonia, amino acids, lactate, and pyruvate, as well as urinaryorganic acids and orotic acid, will identify virtually all of geneticcauses of hyperammonia in this age group. Plasma acylcarnitine profilecan help diagnose various fatty acid oxidation defects. In a fewinstances (carbamyl phosphate synthetase and N-acetylglutamate synthetasedeficiencies), specific enzyme analysis must be performed to confirmdiagnosis. In infantsand children with hyperammonemia, scheme used for neonates can befollowed. However, if urinary organic acids are normal, prothrombintime and serum bilirubin should be measured. If these results areabnormal, liver disease, drugs, hepatotoxins, and Reye syndromeshould be considered. Also, if plasma citrulline is normal, plasmaarginine should be measured. Increase in plasma arginine signifiesarginase deficiency. Low or normal plasma arginine suggests 2 possibilities:lysine protein intolerance or hyperornithinemia-hyperammonemia-homocitrullinemiasyndrome. Increase in urinary lysine signifies lysine protein intolerance,whereas increase in plasma ornithine and urinary homocitrulline signifieshyperornithinemia-hyperammonemia-homocitrullinemia syndrome. Otherinvestigations depend on clinical findings and results of abovetests.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Level of consciousness, decreased:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Try to obtain history information from the patient, if he's alert, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient's behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because a decreased LOC can result from a disorder affecting any body system, tailor the remainder of your evaluation according to the patient's associated symptoms.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Syncope:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur? Obtain a complete drug history.
Next, take the patient's vital signs and examine him for any injuries that may have occurred during his fall. Place him on a cardiac monitor and assess his heart rhythm for abnormalities. Assess cardiac and respiratory status. Monitor pulse oximetry. Perform a neurologic examination.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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